PMID- 27572666
OWN - NLM
STAT- MEDLINE
DCOM- 20170410
LR  - 20170410
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 14
IP  - 4
DP  - 2016 Oct
TI  - TRIF is a regulator of TLR2-induced foam cell formation.
PG  - 3329-35
LID - 10.3892/mmr.2016.5647 [doi]
AB  - The activation of toll-like receptor 2 (TLR2) stimulates foam cell formation, 
      which is a key early event in the process of atherosclerosis. In the present 
      study, the role of toll/interleukin-1 receptor-domain-containing adaptor-inducing 
      interferon-beta (TRIF) in TLR2-mediated foam cell formation was investigated, and 
      the importance of monocyte chemoattractant protein‑1 (MCP‑1), tissue factor (TF) 
      and lectin‑like oxidized low‑density lipoprotein receptor‑1 (Lox‑1) were 
      examined. Treatment of Raw 264.7 cells with the TLR2 agonist. Pam3CSK4, increased 
      the gene expression of TRIF in a time‑dependent manner (RT‑PCR). The induced gene 
      expression of TRIF stimulated by TLR2 was not observed in TLR2‑knockout 
      mice‑derived bone marrow‑derived macrophages (BMDMs). Pam3CSK4 increased the mRNA 
      expression of TRIF in the wild‑type BMDMs, but not in the TLR2‑knockout BMDMs. 
      Knockdown of the expression of TRIF using small interfering RNA decreased 
      Pam3CSK4‑induced foam cell formation (combination of oil‑red O and hematoxylin 
      staining), suggesting a role of TRIF. Stimulation of TLR2 increased the 
      expression levels of various genes, which are known to control atherosclerosis, 
      including MCP‑1, TF and Lox‑1. The knockdown of TRIF also attenuated the 
      Pam3CSK4‑induced expression of these genes. In addition, a reduction in TRIF 
      affected the Pam3CSK4‑induced protein expression of MCP‑1 (EIA). Taken together, 
      the results of the present study suggested that TRIF regulated foam cell 
      formation via regulation of the expression levels of MCP‑1, TF and Lox‑1.
FAU - Huang, Bin
AU  - Huang B
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam 
      University, Daegu 705‑703, Republic of Korea.
FAU - Park, Dae-Weon
AU  - Park DW
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam 
      University, Daegu 705‑703, Republic of Korea.
FAU - Baek, Suk-Hwan
AU  - Baek SH
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam 
      University, Daegu 705‑703, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20160819
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Adaptor Proteins, Vesicular Transport)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Olr1 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Scavenger Receptors, Class E)
RN  - 0 (TICAM-1 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 9035-58-9 (Thromboplastin)
SB  - IM
MH  - Adaptor Proteins, Vesicular Transport/genetics/*immunology
MH  - Animals
MH  - Atherosclerosis/genetics/immunology
MH  - Chemokine CCL2/genetics
MH  - Foam Cells/*immunology/metabolism
MH  - Macrophages
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - RAW 264.7 Cells
MH  - RNA Interference
MH  - RNA, Messenger/genetics
MH  - RNA, Small Interfering/genetics
MH  - Scavenger Receptors, Class E/genetics
MH  - Thromboplastin/genetics
MH  - Toll-Like Receptor 2/*immunology
MH  - Up-Regulation
EDAT- 2016/08/31 06:00
MHDA- 2017/04/11 06:00
CRDT- 2016/08/31 06:00
PHST- 2015/06/30 00:00 [received]
PHST- 2016/04/20 00:00 [accepted]
PHST- 2016/08/31 06:00 [entrez]
PHST- 2016/08/31 06:00 [pubmed]
PHST- 2017/04/11 06:00 [medline]
AID - 10.3892/mmr.2016.5647 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Oct;14(4):3329-35. doi: 10.3892/mmr.2016.5647. Epub 2016 Aug 
      19.